Hormonal
Sodium butyrate supplementation prevents high-fat diet-induced obesity and insulin resistance in mice by inducing epigenetic repositioning of the -1 nucleosome in nuclear-encoded mitochondrial genes, thereby restoring skeletal muscle mitochondrial adaptation and complete beta-oxidation.
In this mouse model, adding sodium butyrate to a high-fat diet prevented obesity and insulin resistance by changing how mitochondrial genes were expressed in muscle. This suggests that sodium butyrate might help mitigate the metabolic damage of a poor diet by improving muscle energy processing, independent of calorie counting.
NaB treatment may be an effective pharmacological approach for type 2 diabetes and obesity by inducing -1 nucleosome repositioning within nuclear-encoded mitochondrial genes, causing skeletal muscle mitochondrial adaptations that result in more complete beta oxidation and a lean, insulin sensitive phenotype.
Why this rating
High-quality mechanistic data (MNase-seq, metabolomics) in a controlled animal model, but results are not directly translatable to humans without further clinical trials.
Source
Sodium butyrate epigenetically modulates high‐fat diet‐induced skeletal muscle mitochondrial adaptation, obesity and insulin resistance through nucleosome positioning
Tara M. Henagan et al. · British Journal of Pharmacology · 2015
DOI 10.1111/bph.13058
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